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Normal islet vascularization is dispensable for expansion of beta-cell mass in response to high-fat diet induced insulin resistance.

Abstract：

:The inability to increase of islet mass adequately to compensate for the demand of insulin due to insulin resistance is an important pathophysiological feature of type 2 diabetes. Previous studies suggested a relationship between pancreatic beta-cell mass and islet vascularization, although no evidence has confirmed this association in response to insulin resistance. Vascular endothelial growth factor-A (VEGF-A) in islets is essential for maintaining normal islet blood vessels. Here, insulin resistance was induced in mice carrying a beta-cell-specific VEGF-A gene mutation (RIP-Cre:Vegf(fl/fl)) by 20-week feeding of high-fat diet as a model of impaired islet vascularization. These mice showed only a modest decrease in glucose tolerance, compared with control mice. In addition, although the endothelial cell area in the islets of high-fat-fed RIP-Cre:Vegf(fl/fl) mice remained diminished, the pancreatic beta-cell area was modestly more than in high-fat-fed control mice. Thus, normal islet vascularization does not seem to be essential for expansion of beta cell mass in response to insulin resistance.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Toyofuku Y,Uchida T,Nakayama S,Hirose T,Kawamori R,Fujitani Y,Inoue M,Watada H

doi

10.1016/j.bbrc.2009.03.138

subject

Has Abstract

pub_date

2009-06-05 00:00:00

pages

303-7

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)00624-X

journal_volume

383

pub_type

杂志文章

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